All organs in the body originate from relatively simple structures in the embryo. For example a simple epithelial tube, the neural tube, develops into the highly complex brain. The many forces and growth factors that act upon embryonic tissues are precisely coordinated to shape the morphogenesis of more complex structures. We are interested in understanding how signalling centres are established in the embryo and how signalling pathways are regulated during development. Current research projects in the lab primarily focus on the fibroblast growth factor (FGF) signalling pathway and our aim is to understand how deregulated FGF signalling results in birth defects and cellular malfunction. We are particularly interested in elucidating the functions of the Sprouty genes, which encode FGF antagonists; Tbx1, a T-box transcription factor implicated in DiGeorge syndrome and Chd7, a chromatin remodeller, mutated in CHARGE syndrome.

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All organs in the body originate from relatively simple structures in the embryo. For example a simple epithelial tube, the neural tube, develops into the highly complex brain. The many forces and growth factors that act upon embryonic tissues are precisely coordinated to shape the morphogenesis of more complex structures. We are interested in understanding how signalling centres are established in the embryo and how signalling pathways are regulated during development. Current research projects in the lab primarily focus on the fibroblast growth factor (FGF) signalling pathway and our aim is to understand how deregulated FGF signalling results in birth defects and cellular malfunction. Our most recent research identified haploinsufficiency of Chd7, a chromatin remodelling factor mutated in CHARGE syndrome, as a potential cause for cerebellar vermis hypoplasia and identified deregulated FGF signalling as the underlying mechanism.

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== Chromatin remodelling in neural development and autism ==

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Haploinsufficiency of the chromatin remodelling factors, CHD7 and CHD8, have been associated with the development of autism spectrum disorders (ASDs). We are using a range of in vivo models and in vitro approaches to understand the function of these factors in brain development and to elucidate the mechanisms whereby insufficiency of these factors might cause autism.

Contents

Welcome to the Basson lab at King's College London

Our research is aimed at uncovering the epigenetic mechanisms that control brain development and underlie neurodevelopmental disorders

The Basson laboratory is located on the 27th floor of Guy's Hospital in the Department of Craniofacial and Stem Cell Biology and affiliated with the MRC Centre for Developmental Neurobiology on Guy's Campus [1]

FGF signalling in development and disease

All organs in the body originate from relatively simple structures in the embryo. For example a simple epithelial tube, the neural tube, develops into the highly complex brain. The many forces and growth factors that act upon embryonic tissues are precisely coordinated to shape the morphogenesis of more complex structures. We are interested in understanding how signalling centres are established in the embryo and how signalling pathways are regulated during development. Current research projects in the lab primarily focus on the fibroblast growth factor (FGF) signalling pathway and our aim is to understand how deregulated FGF signalling results in birth defects and cellular malfunction. Our most recent research identified haploinsufficiency of Chd7, a chromatin remodelling factor mutated in CHARGE syndrome, as a potential cause for cerebellar vermis hypoplasia and identified deregulated FGF signalling as the underlying mechanism.

Chromatin remodelling in neural development and autism

Haploinsufficiency of the chromatin remodelling factors, CHD7 and CHD8, have been associated with the development of autism spectrum disorders (ASDs). We are using a range of in vivo models and in vitro approaches to understand the function of these factors in brain development and to elucidate the mechanisms whereby insufficiency of these factors might cause autism.

In the press

Our work on the cerebellum and autism features in a new article in International Innovation: